Newberg L A
Ann Emerg Med. 1984 Sep;13(9 Pt 2):853-6. doi: 10.1016/s0196-0644(84)80459-x.
Brain protection is the prevention or amelioration of neuronal damage occurring after a hypoxic or ischemic event. Controversies in this field focus on whether incomplete global ischemia may produce a worse insult than does complete global ischemia; whether barbiturates provide protection following complete global ischemia; and whether the calcium entry blockers have a role in brain protection. Current knowledge dictates that incomplete ischemia coupled with hyperglycemia will cause a severe cerebral lactic acidosis and produce a worse insult than does complete ischemia. In the absence of hyperglycemia complete cerebral ischemia produces more neuronal damage. The barbiturates have been shown to provide protection in focal ischemia and incomplete global ischemia in which neuronal function is still present, but have not been shown to provide protection following complete global ischemia. Those calcium entry blockers with cerebral vascular selectivity may well provide some brain protection following complete cerebral ischemia by ameliorating the postischemic hypoperfusion state.
脑保护是指预防或减轻缺氧或缺血事件后发生的神经元损伤。该领域的争议集中在不完全性全脑缺血是否比完全性全脑缺血造成更严重的损害;巴比妥类药物在完全性全脑缺血后是否具有保护作用;以及钙通道阻滞剂在脑保护中是否发挥作用。目前的知识表明,不完全性缺血合并高血糖会导致严重的脑乳酸酸中毒,并比完全性缺血造成更严重的损害。在没有高血糖的情况下,完全性脑缺血会导致更多的神经元损伤。巴比妥类药物已被证明在局灶性缺血和不完全性全脑缺血(其中神经元功能仍然存在)中具有保护作用,但在完全性全脑缺血后尚未显示出具有保护作用。那些具有脑血管选择性的钙通道阻滞剂很可能通过改善缺血后低灌注状态,在完全性脑缺血后提供一定的脑保护作用。